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Health Assessment > Neuro > Flashcards

Neuro Flashcards

1
Q

Multiple Sclerosis pathophys

A

progressive, autoimmune demylelination of central nerve fibers

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2
Q

onset of MS

A

20-40

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3
Q

risk factors for MS

A

female
1st degree relative
Epstein Barr Virus
other autoimmune disorders
smoking

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4
Q

triggers for MS

A

stress
elevated temps
postpartum period

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5
Q

s/s of MS

A

motor weakness, sensory disorders, visual impairment, autonomic instability
varies based on site of demyleination

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6
Q

treatment for MS

A

no cure
managed by corticosteroids, immune modulators, targeted antibodies

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7
Q

pre-anesthetic considerations for MS

A

assess existing deficits
if respiratory compromise - consider PFTs
Labs: CBC with platelets, BMP w/wo LFT
consider preop steroids
temperature management is crucial
avoid succinycholine

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8
Q

why might you draw a BMP with LFT on a MS patient

A

on dantrolene and azathioprine - causes bone marrow suppression, liver function impairment
*close attention to glucose and electrolyes as steroids may impact levels

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9
Q

what anesthetic plan might you have for a MS patient

A

General, regional, peripheral nerve block are acceptable options

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10
Q

what RSI agent would you avoid in MS

A

succinycholine - may induce HyperK+

upregulation of nACh receptors

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11
Q

what might hyperthemia do to an MS patient

A

preciptate an exacerbation of MS symptoms

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12
Q

Myasthenia Gravis Pathophysiology

A

autoimmune: antibodies generated against N-ACh-receptors at skeletal motor endplate
*no effect on smooth or cardiac muscle

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12
Q

which cranial nerves are commonly affected by myasthenia gravis? what effects do they have?

A

ocular (common) - diplopia, ptosis
bulbar - laryngeal/pharyngeal weakness leading to respiratory insuffiency, aspiration risk

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12
Q

when is maysthenia gravis (MG) muscle weakness exacerbated

A

w/ exercise

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13
Q

thymic hyperplasia in myasthenia gravis is common at _____% with _____% of patients improving with thymectomy

A

thymic hyperplasia in myasthenia gravis is common at 10% with 90% of patients improving with thymectomy

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14
Q

what can cause symptom exacerbation with myasthenia gravis

A

pain, insomnia, infection, surgery

stress

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15
Q

treatment of myasthenia gravis

A

ACh-E inhibitors (pyridostigmine), immunosuppressive agents, steroids, plasmapharesis, IVIG

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16
Q

MG preanesthetic considerations

A

assess existing deficits
if respiratory compromise, consider PFTs
optimize respiratory function
Labs: CBC, BMP +/- LFT
counsel pt on increased risk of postop vent support until fully recovered from anesthesia

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17
Q

4 medication considerations with MG

A
  • reduce NMB dose to avoid prolonged muscle weakness
  • caution with opioid to avoid respiratory compromise
  • ACh-E inhibitors prolong succinycholine and ester LAs (X-caine)
  • preop steroid with anyone on long term steroids
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18
Q

when would you add an LFT to MG chem panel

A

if the patient is on azathiporine

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19
Q

eaton-lambert syndrome pathophysiology

A

autoantibodies against VG Ca++Channels
-reduce Ca++ influx decreasing ACh release at the NMJ

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20
Q

> 60% of eaton lambert syndrome cases are associated with what

A

small cell lung carcinoma

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21
Q

s/s of Eaton Lambert Syndrome

A

progressive limb-girdle weakness, dysautonomia, oculbulbar palsy

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22
Q

treatment for eaton lambert syndrome

A

Selective K+ channel blocker
“3-4 diaminopyridine”
ACh-E inhibitors
Aziathioprine (immunologics)
Steroids
Plasmapheresis, IVIG

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23
Q

preanesthetic considerations for ELS (Eaton Lambert Syndrome)

A

assess exsisting deficits
if respiratory compromise - PFTs
optimize respiratory functoin
*extreme caution with NMB and opioid dosing
may need post-op respiratory support until fully recovered from anesthesia

consider regional

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24
Q

ELS and neuromuscular blockers

A

VERY SENSITIVE to ND-NMB and D-NMB
*significantly more sensitive to ND-NMB than MG patients

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25
Q

muscular dystophy pathophysiology

A

hereditary disorder of msucle fiber degerneration caused by breakdown of the dystophin-glycoprotein complex
- leading to myonecrosis, fibrosis, and skeletal membrane permeability

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26
Q

what is the most common and severe form of muscular dysrophy
who does it affect- onset & lifespan

A

Duchenne (DMD)
occurs only on boys, onset 2-5y
Wheelchair bound by 8-10 y
lifespan ~20-25 d/t cardiopulm complications

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27
Q

s/s of muscular dystrophy

A

progressive skeletal muscle wasting without motor/sensory abnormalities, kyphoscolosis, long bone fragility, respiratory weakness, frequent PNE, EKG changes

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28
Q

what lab is elevated in muscular dystrophy and why?

A

creatine kinase due to muscle wasting

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29
Q

what is myotonia

A

prolonged contractions after muscle stimulation, seen in several muscle disorders

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30
Q

most common myotonia

A

myotonic dystrophy
onset: 20-30 years
muscle wasting in face, masseter, hand, pre-tibial muscles & may effect pharyngeal, laryngeal, diaphragmatic muscles
cardiac conduction may be effected

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31
Q

what valvular disorder is seen in myotonic dystrophy

A

20% have mitral valve prolapse

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32
Q

myotnia congenita involves what muscles

A

involves skeletal (smooth/ cardiac muscles are spared)

(milder form)

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33
Q

what is central core disease

A

rare. core muscles cells lack mitochondrial enzymes
- proximal muscle weakness & scoliosis

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34
Q

what triggers myotonias

A

stress and cold temps

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35
Q

treatment for myotonias

A

no cure
managed with quinine, procainamide, steroids

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36
Q

preanesthetic condiserations for muscular dystrophies

A

CBC, BMP, PFTs, consider CK
preop EKG, ECHO - elvaluate for cardiomyopathy

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37
Q

drug condiserations for muscular dystrophies

A

caution with Non-depolarizing NMB (careful montiroing throughout)
hypermetabolic syndrome - similar to MH seen with sux and volatile anesthetics
can lead to rhabdo, HyperK+, vfib & cardiac arrest
Sux and VA may exacerbate instability of muscle membrane

consider lose dose Roc and TIVA for GA, Have MH cart with dantrolene available

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38
Q

pre anesthetic considerations for myotonic dystrophy (9)

A
  • assess extent of CV and pulmonary abnormalities
  • assess breath and heart sounds
  • GI hypomotility (aspiration risk)
  • high reaction of endocrine abnormalities (check thyroid and glucose levels)
  • keep warm to avoid flares
  • avoid Depolarizing NMB b/c fasiculations trigger myotonia
  • caution with opioids
  • optimize respiratory status
  • incerased risk of postop respitatory weakness
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39
Q

3 major dementia syndromes

A

alzheimers (70%)
Vascular dementia (25%)
parkinsons (5%)

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40
Q

basic preop consierations with dementia patients

A

assess baseline level of cognitive dysfunction
- if patient unable to give informed consent look to medical POA
- investigate any advanced directives for medical decision making
- review basic labs and pertinent test/imaging
- potential aspiration risk (may be full stomach)
- increased risk for postop delirium (consider TIVA)

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41
Q

which preop meds need to be reviewed prior to anesthetic with dementia patients

A

ACh-I, MAOIs, psych meds

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42
Q

preferred anesthetic plan on dementia patietns

A

regional - decreased opioid requirement
balance opioids to meet analgesic requirement without exacerbating delirium

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43
Q

parkinson’s disease pathophysiology

A

degeneration of dopaminergic fibers of basal ganglia
unknown case. advanced age is the biggest risk factor

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44
Q

dopamine regulates the _________ by ____ _____ stimulation, which is stimulated by _______

A

dopamine regulates the extrapyramidal motor system by inhibiting exess stimulation, which is stimulated by ACh

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45
Q

T/F in parkinsons the motor neurons are under stimulated

A

false, in parkinon’s motor neurons are over stiumulated

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46
Q

triad of symptoms with parkinsons

A

skeletal muscle tremor, rigitidity, akinesia, posture
TRAP

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47
Q

other symptoms of parkinsons

A

pill roll tremor, facial rigidity, slurred speech, difficulty swallowing, respiratory difficutlty, depression, and dementia

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48
Q

treatment for parkinsons

A

Levadopa (cross BBB), anticholinergics, MAOIs (inhibit dopamine degredation), deep brain stimulator

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49
Q

preanesthetic considerations for parkinsons

A

assess severity with special attetention to respiratory compromise
review home meds (MAOIs)
basic labs along with PFT if respiratory symptoms
EKG, ECHO if indicated
increased aspiration risk (dysphagia, or possible dementia)

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50
Q

mediations to avoid in parkinsons patients

A

avoid reglan, phenothiazines, butyrophenones
avoid demerol if on MAOI

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51
Q

parkinsons home med to continue prior to surgery

A

PO levadopa must be continued to avoid unstable extrapyramidal effects such as chest wall rigidity

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52
Q

parkinsons patient with Deep brain stimulator considerations

A
  • DBS may need to be disabled to avoid interaction with cautery
  • if cautery used, biopolar recommended
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53
Q

in regards to brain tumors what can cause neurologic deficits

A

the mass effects!
increases ICP, papilledema, headache, mental impairment, mobility impairment, vomiting, autonomic dysfunction, seizures

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54
Q

brain tumors - pre anesthesia considerations

A

history, previous therapies, presenting symptoms & neurological deficits
radiation damage may lead to lethargy and AMS
chemoteraphy may also have neuro effects
CBC, BMP (glucose), EKG
CT/MRI
preop steroids and antiseizure per surgeon

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55
Q

why are patients w brain tumors on steroids

A

minimize cerebral edema
*continue steroids and monitor glucose

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56
Q

what diuretic is used to reduce ICP and pressure

A

mannitol

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57
Q

autonomic dysfunction from brain tumor may manifest on

A

EKG
labile HR and BP

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58
Q

anticonvulsants are common with which lesions

A

supratentorial lesions closer to motor cortex

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59
Q

cerebrovascular disease preop considerations

A
  • review history, deficits, imaging, treatments, and co-existing disease
  • assess orientation, pupils, bilateral grip stregnth, LE strength
  • ask about headache, tinnitus, vision/memory loss, bathroom issues
  • assess cause of CVA - vascular, embolic
  • Imaging- carotid U/S, CT/MRI head and neck and ECHO
  • preop EKG
  • CBC, BMP (including glucose)
  • cerebral oximetry
  • Aline, 2 IV and/or CVC
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60
Q

causes of embolic CVA

A

afib, prostethic valve, right to left shunt, PFO

61
Q

new anticoagulant use for cardiac thrombus means what

A

no elective cases within 3 months

62
Q

if pt is on anticoagulant for CVA prophylaxis

A

consult prescriber to establish protocol

63
Q

high risk patients on long acting anticoags need what to bridge the gap

A

short acting anticoagulants (LMWH, IV unfractionated heparin)
*close monitoring of coagulation status is required

64
Q

can you do regional anesthesia on a pt with CVA history and anticoags

A

if anticoags have been D/Cd for sufficient time to perform block

65
Q

clincal manifestations of regional strokes - anterior cerebral artery

A

contralateral leg weakness

66
Q

1.

clincal manifestations of regional strokes - middle cerebral artery

A

contralateral hemiparesis and hemisensory deficits (face and arm more than legs)
aphasia (dominant hemisphere)
contralaterral visual defect

67
Q

clincal manifestations of regional strokes - posterior cerebral artery

A

contralateral visual vield defect
contralateral hemiparesis

68
Q

clincal manifestations of regional strokes - penetrating arteries

A

contralateral hemiparesis
contralateral hemisensory deficits

69
Q

clincal manifestations of regional strokes - basilar artery

A

oculomotor deficits and or ataxia with crossed sensory and motor deficits

70
Q

clincal manifestations of regional strokes - veterbal artery

A

lower cranial nerve deficits and or ataxia with crossed senory deficits

71
Q

majority of aneurysms not diagnosed before _____

A

rupture
* only 1/3 aneursyms pts have sx before rupture

72
Q

s/s of cerebral aneursym

A

headache, photophobia, confusion, hemiparesis, coma

73
Q

risk factors for cerebral aneursym

A

HTN
smoking
female
oral contraceptive
cocaine use

74
Q

diagnosis of cerebral aneursym

A

CT/angio
MRI
lumbar puncture with CSF analysis (if rupture suspected)

75
Q

intervention for cerebal aneurysm should be preformed within how many hours of rupture for best outcome

A

72 hours

76
Q

pre-anesthesia considerations for cerebral aneursyms

A

CT/MRI, EKG, ECHO, CBC, BMP, T&C with blood available
*BP control, mannitol (avoid rupture)
*seizure prophylaxis
*CVC

77
Q

surgical treatment of cerebral aneursyms

A

coiling, stenting, trapping, bypass (very large aneursyms)
*Neurosurgery on standby incase of intraop rupture/SAH

78
Q

T/F pts with cerebral aneurysms may be on steroids

A

True, monitor glucose

79
Q

when are vasospasms likely to occur post Sub archonid hemorrage (SAH)

A

3-15 days post SAH

80
Q

triple H therapy for SAH vasospasm

A

hypertension
hypervolume
hemodilution
*to avoid complications of hypervolemia, HTN is the initial main treatment

81
Q

interventional treatment for post SAH vasospasm

A

balloon dilation
direct injection of vasodilators to relieve the vasospasm

82
Q

aneursym grading for prognosis

A

Hunt & Hess
0- unruptured
1- reputrued with minimal headdache and no neuro deficits
2- moderate to sever headache, no deficit other than cranial nerve palsy
3- drowsiness, confusion, mild focal motor deficit
4- stupor, significant hemiparesis, early decebration
5 - deep coma, decebrate rigidity

83
Q

what is an AVM

A

aterial to venous connection without intervening capillaries
*high flow, low resistance shunting
*believed to be congetinal

84
Q

symtpoms of AVM

A

range from mass-effects to hemorrhage

85
Q

where are majority of AVM located

A

supratentorial

86
Q

diagnosis of AVM

A

angio, MRI

87
Q

treatment of AVM

A

radiation, angio-guided embolization
surgical resection (higher mortality)

88
Q

pre anesthesia considerations for AVM

A

H&P, review meds, imaging, CBC, BMP, T&C, EKG, ECHO
*BP control, seizure prophalyxsis (supratentorial)
*large bore IV access x2 or CVC, Aline

89
Q

traumatic brain injury “TBI” severity is categorized by

A

GCS - glascow-coma scale

90
Q

secondary injuries- TBI (6)

TBI (traumatic brain injury)

A

neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, neurogenic shock

90
Q

primary injury -TBI

TBI (traumatic brain injury)

A

occurs at time of insult

91
Q

intubation is required in severe TBI

A

GCS <9
Airway trauma
respiratory distress

92
Q

mild hyperventilation to control

A

ICP

93
Q

pre anesthesia considerations for TBI

A

do not delay emergent surgery
review co-morbidities, degree of injury, imaging, labs, gross neuro exam
*C-Spine stabilization, IV access, CVC, ALine, possible uncrossmatched blood if no time for T&C
*intraop ISTAT, pressors, bicarb, Calcium, blood products

94
Q

why to refrain from NGT/OGT in TBI

A

potential basal skull fracture

95
Q

chari malformation

A

congential displacement of cerellum
C/o Headache, extending to shoulders/arm, visual disturbances, ataxia
Tx= surgical decompression

96
Q

pre-anesthesia considerations for Chari malformation

A

Review H&P, deficits, imaging, CBC, BMP, T&C
May hyperventilate to ↓ICP, Lg bore IV x 2 or CVC, Aline

97
Q

classifications of Chiari Malformation

A

Type I - downward displacement of cerebellum
Type 2 - downward displacement of cerebellar vermis, often assoiated with myelomeningocele
Type 3 - rare
Type 4 - not compatible with life

98
Q

Pre-anesthesia considerations for seizures

A

Determine source of seizures (if known) and how well they are controlled.
Want anti-seizure drugs on board before incision.
Review drugs and pharmacokinetic/pharmacodynamic actions

99
Q

May be called to intubate post-seizure

A

RSI w/cricoid pressure

100
Q

seizure
& causes

A

transient, paroxysmal, and synchronous discharge of neurons in the brain
caused by transient abnormalities: hypoglycemia, hyponatremia, hyperthermia, intoxication
-In these cases, treating the underlying cause is curative

101
Q

Epilepsy

A

recurrent seizures d/t congenital or acquired factors

102
Q

Antiepileptic drugs decrease ____ excitability/enhance _____

A

Antiepileptic drugs decrease neuronal excitability/enhance inhibition

103
Q

which seizure drugs cause drug-drug interactions

A

Phenytoin, Tegretol, Barbiturates are enzyme-inducers

may need a larger dose

104
Q

Cerebral Blood Flow is modulated by

A

cerebral metabolic rate
cerebral perufsion pressure (CPP = MAP - ICP)
PaCO2
PaO2
various drugs and intracranial pathologies

105
Q

with autoregulation CBF is approximately _____ mL/100g brain tissue per minute

A

50 mL/100g brain tissue per minute
750 mL/min
15% cardiac output

106
Q

the intracranial and spinal vault is enclosed by what? what are the contents in the vault

A

neural tissue (brain + spinal cord), blood, and CSF
enclosed by dura mater and bone

107
Q

under normal conditions what is the volume of brain tissue, intracranial CSF, and intracranial blood and ICP

A

1200-1500 mL
at this volume ICP = 5-15 mmHg

108
Q

what is the monroe kellie hypothesis

A

any increase in one component of intracranial volume must be offset by a decrease in another component to prevent elevated ICP

109
Q

what happens if the compensation for decreasing ICP fail

A

cerebral ischemia

110
Q

falx cerebri seperates what

A

the 2 cerebral hemispheres

111
Q

the tentorium cerebelli is a reflection of dura that lies rostral to the cerebellum and marks the border between the

A

supratentorial and infratentorial spaces

112
Q

increases in contents of one region may cause regional increases in ICP and in extreme instance the contents can

A

herniate into a different compartment

113
Q

subfalcine herniation

A

herniation of hemispheric contents under the flax cerebri
typically compressing branches of the anterior cerebral artery, creating a MLS

midline shift (MLS)

1

114
Q

transtentorial herniation

A

herniation of the supratentorial contents past the tentorium cerebelli causing brainstem compression in a rostral to caudal direction

2

115
Q

uncal herniation

A

subtype of transtentorial herniation

uncus (medial portion of temporal lobe) herniates over the tentorium cerebelli

4

116
Q

signs of uncal herniation

A

ipsilateral oculomotor nerve dysfunction
*pupillary dilation, ptosis, lateral deviation of the affected eye, brainstem compression, death

117
Q

herniation of cerebellar tonsils

A

occur due to elevated infratentorial pressure causing the cerebellar structure to herniate through the foramen magnunm

3

118
Q

symptoms of herniation of cerebellar tonsils

A

medullary dysfunction, cardiorespiratory instability death

119
Q

causes of increased ICP

A

tumors
intracranial hematomas
infections - meningitis or encephalitis

120
Q

how do tumors contribute to increased ICP

A

directly bc of their size (space-occupying lesions)
inderectly by causing edema in surrounding tissue
obstructing CSF flow, as seen with tumors involving the 3rd ventricle

121
Q

how to do intracranial hematomas increase ICP

A

obstruction of CSF reabsorption
and granulations

122
Q

methods to decrease ICP

A
  • elevate HOB to encoruage jugular venous outflow
  • hyperventilation
  • CSF drainage (EVD)
  • hyperosmotic drugs
  • diuretics - induce. systemic hypovolemia
  • corticosteroids - decrease swelling and the integrity of BBB
  • cerebral vascocontricting agents(prop- decreases CMRO2 and CBF)
  • surgical decompression
123
Q

neuro assessment

A

preop and postop neuro assessment
review imaging, current meds/treatment

124
Q

which anesthetic plan is preferred with muscular dystrophies

A

RA > GA to avoid trigers and cardiopulmonary complications

125
Q

astrocytomas

A

most common CNS glial cells
*gliomas
pilocytic astrocytomas
anaplastic astrocytomas
glioblastoma multiforme

126
Q

gliomas

A

primary tumors, least aggresive astrocytomas - found in young adults with new onset seizure

127
Q

pilocytic astrocytomas

A

children and young adults
mostly benign, good outcomes if resected

128
Q

anaplastic astrocytomas

A

poorly differentiated
ususally eveolve into glioblastoma multiforme

129
Q

glioblastoma multiforme

A

carry a high mortality rate
usualy require surgical debulking and chemo
life expectancy is usually within weeks even with treatment

130
Q

menigiomas

A

usually benign, arise from dura or arachnoid tissue
*good prognosis with surgical resection

131
Q

pituitary adenomas

A

noncancerous, varying subtypes
transphenodial or open cranitomy for removal is usually curative

132
Q

acoustic neuromas

A

usually benign schawnnomas involving vestiular component of CN VIII within auditory canal
good prog with resection +/- radiation

133
Q

metastatic carcinomas

A

vary widely in orgin and symptoms
outcomes generally less favorable

134
Q

blood is supplied to the brain from

A

internal carotids and vetebral arteries

these vessels join on the inferior surface of the brain to form the circle of willis, which during ideal circumstances provides collateral circualtion to multiple areas of the brain

135
Q

TIA

transiet ischemic attack

A

sudden focal vascular, neurologic deficit that resolves within 24 hour
1/3 patients who experience a TIA will subsequently suffer a stroke
stoke prognosis depend on time from onset thrombolytic intervention (<90min)

136
Q

suspected stroke requires

A

stat non-contrast CT due r/o intracerebral hemorrhage

137
Q

causes of ischmemic stroke are categorized according to the TOAST classifications

A

Large artery atherosclerosis (carotid stenosis)
Small vessel occlusion (lacunar stroke)
Cardioaortic embolic (afib emboli)
other eitology (hypercoaguable or vasculopathy)
undetermined etiology

138
Q

recommended treatment for acute ischemic stroke

A

PO aspirin - initial
IV or intra-arterial tPA when criteria are met within a limite time window
thrombectomy
revascularization

139
Q

pre-anesthetic considerations for ischemic CVA

A

avoid delay in treatment
baseline neuro assessment, CV function, ability to lie flat
airway needed?
patients with ischemic stroke frequently have CV risk factors (HTN, DM, CAD, AFib, valvular disease) and can impact vasoactive drug choices and hemodynamic goals

140
Q

hemorrhagic CVA treatment

A

depends on severity
conservative treatment is centered around reducing ICP, BP control, seizure precautions and vigilant monitoring
surgical treatment for evacuation of hematoma
intubation depending on cardiopulm status
ICU monitoring

141
Q

2 reliable predictors of outcomes for hemorrhagic CVA

A

estimated blood volume and change in LOC

142
Q

subtypes of hemorrhagic strokes

A

IPH - intraparychemal - blood within the brain
epidural - epidural space
subdural - subdural space
SAH - subaracnoid space
IVH - intraventricular - within the ventricular system

IVH usually occur in conjunction with other types of hemorrhagic stroke

143
Q

cause of vasospasm with SAH

A

free Hgb tiggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1 leading to vasoconstriction

144
Q

hydrocephalus

A

disorder of CSF accumulation causing increased ICP resulting in ventricualr dilation

imbalance between production and absorption

145
Q

causes of hydrocephalus

A

congenital or acquired due to meningitis, tumors, head injury, stroke

146
Q

treatment for hydrocephalus

A

diuretics (furesomide and acetazolamide decrease CSF production)
serial lumbar punctures (temporzing measure)
VP shunt - drain placed in ventricle and empties in peritoneum
Endoscopic Thrid Ventriculostomy - catheter placed into lateral ventricle and drains into peritoneal space, Right atrium, or pleural space

147
Q

neurofibromatosis

A

autosomal dominant
3 types (type I most common)
numerous disease presentations
Anesthesia considerations account for increased ICP, airway issues, scolisis, and the possibility of pheochromocytoma

avoid neuraxial due to high likelihood of spinal tumors

148
Q

von hippel-lindau disease

A

autosomal dominant
benign tumors of the CNS, eye, adrenals, pancreas and kidneys
may present with pheochromocytoma
anesthesia considerations take into account exaggerated HTN

Neuraxial may be limited if there is co-existing spinal cord tumor

149
Q

tuberous sclerosis

AKA Bourneville Disease

A

autosomal dominant disease causing beingn hemartomas,, angiofibromas and other malformations occuring in the body
lesions of the brain include cortical tumors and giant-cell astrocytomas

150
Q

presentation of tuberous sclerosis and anesthesia considerations

A

mental retardation and seizure disorders
anesthesia make take into account airway compromise, kidney or cardiac involvement

Health Assessment (16 decks)

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